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Biomedical subjects

D Catovsky

Publications and source records attributed to D Catovsky.

At least 343 records · Page 19Linked to original sources
PubMed1986

Variant translocation t(8;22) and abnormalities of chromosome 15(q22) and 17(q12-21) in a Burkitt's lymphoma/leukaemia with disseminated intravascular coagulation.

Severe disseminated intravascular coagulation was observed in a patient with Burkitt's lymphoma/leukaemia. Immunological studies on leukaemic blasts from relapsed bone marrow revealed a B-cell phenotype (B4+, B1+, HLA-Dr+, J5+) with membrane bound IgM lambda. Cytogenetic investigation revealed a variant Burkitt's translocation t(8;22)(q24;q11) involving the lambda light chain gene region and abnormalities of chromosomes 15 and 17 with breakpoints at q22 and q12 respectively, similar to those observed in the t(15;17) in acute promyelocytic leukaemia. Transmission electron microscopy of the leukaemic blasts showed crystalline cytoplasmic inclusions which may have had a role in precipitating the disseminated intravascular coagulation.

Adult↗
PubMed1986

Chromosome and cell culture studies in eosinophilic leukaemia.

A cytogenetic analysis was carried out on bone marrow cells from 11 patients who presented with hypereosinophilia and the clinical features of the idiopathic hypereosinophilic syndrome. One of these patients was found to have trisomy 8 affecting the myeloid series, including eosinophils. In this patient, marrow eosinophils also showed asynchrony of nuclear-cytoplasmic maturation, and there were increased numbers of myeloid progenitor cells in the blood. Six months later, blast cell transformation occurred, and he died soon afterwards. These findings show that abnormalities in the karyotype of bone marrow cells and culture of blood progenitor cells may help to identity eosinophilic leukaemia among patients who present with features of the idiopathic hypereosinophilic syndrome.

Adolescent↗
PubMed1986

The relationship between chronic lymphocytic leukaemia and prolymphocytic leukaemia. II. Patterns of evolution of 'prolymphocytoid' transformation.

A series of 55 patients with B-cell chronic lymphocytic leukaemia (CLL) and prolymphocytic leukaemia (PLL) was studied in order to investigate the evolution of prolymphocytoid transformation of CLL. Peripheral blood films were assessed for the percentages of prolymphocytes (%PROL) during a followup period of 2 months to 24 years. The majority of patients with typical CLL (less than or equal to 10% PROL) had minor variations or transient increases in %PROL throughout the course of the disease, but in one third of them a steady rise in the proportion of these cells was documented. Patients presenting with 11-55% PROL, referred to as CLL/PL, exhibited three patterns of evolution: half of them showed stability of the PROL counts, one third had unsustained increases in the %PROL and 18% showed definite progression to a PLL-like blood picture. Patients diagnosed as PLL (greater than 55% PROL) had maintained a high %PROL during the period of observation. Serial marker studies in some CLL and CLL/PL cases showed that the percentage of M-rosettes and the intensity of SmIg remained at the same initial levels in all but two cases. These two cases in the CLL/PL group showed a significant decrease in the percentage of M-rosettes and stronger SmIg staining associated with progressive prolymphocytoid transformation. Patients with CLL and CLL/PL who had a sustained rise in the %PROL responded poorly to treatment compared with those with stable disease.

Cell Transformation, Neoplastic↗
PubMed1986

The morphological spectrum of T-prolymphocytic leukaemia.

The morphology of the cells from 29 cases of T-prolymphocytic leukaemia (T-PLL) was studied by light (LM) and transmission electron microscopy (TEM) and was compared with that of 33 B-cell PLL. The membrane phenotype of T-PLL cells was T4+, T8- in two-thirds of the cases, others being T4- T8+ or T4+ T8+. Two morphological types of T-PLL were defined according to the nuclear features: regular (55% of cases) and irregular (45% of cases). T-PLL cells with a regular, round or oval, nuclear outline resembled B-PLL cells but had less abundant cytoplasm and a higher nucleo-cytoplasmic ratio. Irregular T-prolymphocytes displayed a distinct convoluted nucleus. A 'small-cell' variant of T-PLL was recognized by TEM in six cases in which the diagnosis was uncertain by LM. A characteristic of all types of T-prolymphocytes by LM was the presence of a deep basophilic cytoplasm which by TEM corresponded to clusters of ribosomes and endoplasmic reticulum. No differences in clinico-haematological features or membrane markers were apparent between the morphological types of T-PLL, although it was noted that the three T4- T8+ cases had irregular cells and four of the small cell variant were T3- T4+. TEM permits a more precise assessment of the cytoplasmic organelles and nucleolus than LM analysis and facilitates the distinction between T-PLL and other leukaemias with a mature T-cell phenotype, namely adult T-cell leukaemia/lymphoma. Sezary syndrome and T-chronic lymphocytic leukaemia.

Aged↗
PubMed1986

Adult acute lymphoblastic leukaemia presenting with bone marrow aplasia.

We report two adult patients who presented with bone marrow aplasia and latterly were diagnosed to have acute lymphoblastic leukaemia (ALL). Although the aplastic presentation of ALL in childhood is well documented it has not been previously reported in adult ALL. The mechanism of this presentation is unclear. In one of our patients folate deficiency appears to have been the cause.

Acute Disease↗
PubMed1986

Coexpression of T- and B-markers in a lymphoproliferative disorder.

An atypical case of lymphoproliferative disorder in which T- and B-cell antigens were coexpressed in the neoplastic cells is described. The disease was characterised by hepatosplenomegaly, lymphadenopathy, a low WBC (5 X 10(9)/l) and bone marrow infiltration. The predominant cell population (greater than 70%) comprised lymphoid cells with a range of nuclear irregularities and included some blast cells. 90% of the peripheral blood lymphocytes showed a mature T-helper phenotype (E+, T11+, T3+, T4+, T8-, T6-, TdT-) with coexpression of the specific B-markers B1 and FMC7, in 90% and 50% of cells, respectively. HLA-DR antigens were present in 55% of cells while surface and cytoplasmic immunoglobulins (Ig) were detected in less than 10% of cells. Molecular investigations with appropriate probes showed evidence of T-cell receptor gene rearrangement but no rearrangement for the genes of the Ig-heavy and -light chains. Cytogenetic studies revealed a translocation t(10;19) (p12; q13) in all the metaphases analyzed. This case demonstrates that the study of neoplastic cells with a battery of monoclonal antibodies may disclose the existence of a hitherto unrecognised lymphoid cell population with atypical expression of B- and T-cell antigens. On the other hand, the presence of T-cell receptor gene rearrangement indicates that this is a T-cell disorder with the aberrant co-expression of specific B-cell markers.

Aged↗
PubMed1986

Hypercalcaemia in T cell acute lymphoblastic leukaemia: report of two cases.

Two young adults presenting with acute lymphoblastic leukaemia (ALL) associated with hypercalcaemia and osteolytic lesions were both found to have T cell ALL. Hypercalcaemia is a rare feature of ALL and has not previously been related to T cell disease. Both cases, in some respects, resembled (age between 10 and 20 years and low white cell count) the few other previously reported cases. In one of our cases increased concentrations of vitamin D3 seemed to have a role in the pathogenesis of the hypercalcaemia.

Adolescent↗
PubMed1986

Incomplete Reiter's syndrome following chemotherapy of acute myeloid leukaemia.

Reiter's syndrome and other reactive arthritides have been described following infection with various organisms although they can occur in unusual circumstances without an obvious infectious precipitant. We have recently witnessed two attacks of reactive arthritis and keratoderma blenorrhagica occurring in an HLA B27 adult male following chemotherapy on two separate occasions with the same drugs for acute myeloid leukaemia. No attacks occurred before or following the cessation of these drugs. This supports the view that in Reiter's syndrome a common pathogenic pathway is triggered by an 'arthritogenic factor' which in this case appears to have been chemical.

Adult↗
PubMed1986

Abnormalities of chromosome 7q and Tac expression in T cell leukemias.

Clonal chromosome abnormalities were demonstrated in 13 cases of T cell leukemia with a mature membrane phenotype. The cases comprised two adult T cell lymphoma leukemia (ATLL), five Sézary syndrome (SS), three T prolymphocytic leukemia (T-PLL), and three T chronic lymphocytic leukemia (T-CLL). The presence of clonal chromosome abnormalities in the three cases of T-CLL supports the view that although clinically benign, this disorder probably represents a neoplastic process. Cells from six of 11 patients were tested and found to be reactive with monoclonal antibody (McAb) anti-Tac in the absence of mitogens (two ATLL, two SS, and two T-PLL). Only the two ATLL patients were serologically positive for the human T cell leukemia virus I (HTLV-I), and their cells showed a higher anti-Tac reactivity. Chromosome 7 abnormalities were observed in seven cases (two ATLL, three SS, two T-PLL), and a strong correlation was seen between the presence of a 7q abnormality and the expression of the Tac antigen (T cell growth factor receptor). These findings are discussed in relation to the localization of T cell receptor genes on chromosome 7 and possible mechanisms for the activation of the Tac gene.

Antibodies, Monoclonal↗
PubMed1986

Chromosomal abnormalities identify high-risk and low-risk patients with acute lymphoblastic leukemia.

The importance of banded chromosome analyses in predicting long-term outcome in acute lymphoblastic leukemia (ALL) was evaluated in this follow-up study of 329 patients from the Third International Workshop on Chromosomes in Leukemia. Patients were divided into ten groups according to pretreatment karyotype: no abnormalities, one of the following structural abnormalities [the Philadelphia chromosome, translocations involving 8q24,t(4;11), 14q+, 6q-] or, in the remaining cases, modal number [less than 46, 46, 47 to 50, greater than 50]. Achievement and duration of complete remission (CR) and survival differed among chromosome groups (P less than .0001). Karyotype was an independent prognostic factor for duration of first CR and survival, even when age, initial leukocyte count (WBC), French-American-British (FAB) type, and immunologic phenotype were considered. Among adults, prolonged remission and survival were uncommon in all chromosome groups. Only in the normal karyotype group was median survival even two years. Among children, striking differences in long-term remission and survival were seen depending upon karyotype. Children in the greater than 50 group did best, with 70% remaining in first CR for a median duration in excess of five years. Children in the 47-50, 6q-, and normal karyotype groups also had prolonged survivals. In contrast, certain translocations [t(9;22)(q34;q11), t(4;11)(q21;q14-23), t(8;14)(q24;q32)] identified children who had short survivals, even in the presence of favorable prognostic factors including a low WBC, L1 morphology, and non-T, non-B immunologic phenotype. We conclude that chromosome analysis is required at diagnosis in patients with ALL, and that children with these specific translocations should be managed as having high-risk ALL.

Adult↗
PubMed1986

An unusual variant of T-CLL: evidence for the existence of a hitherto unrecognized T cell subset.

A case of T-cell chronic lymphocytic leukaemia (T-CLL) with an unusual mature membrane phenotype: E+, CD3+, CD4+, CD8-, M1+, Leu-15+, Fc gamma+, is described. The cells were large granular lymphocytes with slight immature features. Functionally these cells lacked helper, suppressor and NK activity but possessed normal levels of K activity. These findings demonstrate several features not previously described in T-CLL: the coexpression of the antigens detected by T4, M1 and Leu-15 the presence of Fc gamma receptors on CD4+ lymphocytes and the lack of NK activity in M1+, Fc gamma+ cells. This study broadens the known heterogeneity of T-CLL and suggests the existence of a hitherto unrecognized normal T-lymphocyte subset with the same functional and phenotypic characteristics as in the case described here.

Antibodies, Monoclonal↗
PubMed1986

The relationship between chronic lymphocytic leukaemia and prolymphocytic leukaemia. I. Clinical and laboratory features of 300 patients and characterization of an intermediate group.

The clinical and laboratory features of 300 patients with chronic lymphocytic leukaemia (CLL) and prolymphocytic leukaemia (PLL) of B-cell type were studied in order to investigate the relationship between these two diseases. Statistical analysis demonstrated that more than 55% circulating prolymphocytes (PROL) was a defining criterion for PLL, disorder characterized by marked splenomegaly without lymph-node enlargement, cells with high density of membrane-immunoglobulin (SmIg), low mouse-rosettes (M-rosettes) and strong reactivity with the monoclonal antibody FMC7. Patients with typical CLL, defined as having less than 10% PROL, were on average 10 years younger than those with PLL and showed preferential lymph-node to spleen involvement. Characteristic markers of CLL were weak SmIg, high M-rosettes and low reactivity with FMC7. Patients with 11-55% PROL, group designated as CLL/PL, were found to have intermediate features between CLL and PLL: the degree of splenomegaly was disproportionate to the lymph-node enlargement, the number of cases with strong SmIg was closer to that found in PLL, but the other markers were not significantly different from CLL. The CLL/PL group appeared to be heterogeneous and includes at least two types of CLL, one with increased proportions of PROL but otherwise typical disease, and another in 'prolymphocytoid' transformation. Our study suggests that although PLL cannot be considered as the extreme end of a continuous spectrum from typical CLL, the spleen may be the source of PROL both in PLL and in CLL/PL.

Age Factors↗
PubMed1985

Heterogeneity of T-cell beta-chain gene rearrangements in human leukaemias and lymphomas.

The state of T-cell receptor beta-chain gene rearrangement in human T-cell leukaemias has been analysed. All forms of leukaemia tested (T-CLL, ALL, PLL, Sezary syndrome and ATL) exhibit rearrangements of C beta genes confirming the clonality of these neoplasias. However we find no evidence for common gene rearrangements nor for restricted rearrangement patterns within this type of neoplasia. We find evidence of T-cells with C beta 1 and C beta 2 rearrangements, sometimes associated with Igh JH rearrangements, but several cases of T-cell leukaemia with a marker inversion of chromosome 14 (q11;q32) do not have Igh JH rearrangements. The results suggest that TCR beta gene rearrangement occurs early in T-cell ontogeny but that this rearrangement is most often irrelevant to leukaemogenesis.

Cell Line↗